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Published on: February 21, 2016
Deletion of Oncomodulin Gives Rise to Early Progressive Cochlear Dysfunction in C57 and CBA Mice
Leslie K Climer1, Aubrey J Hornak1, Kaitlin Murtha1
1Department of Biology, Baylor University, Waco, TX, United States.
Abstract:
Ca2+ signaling is a major contributor to sensory hair cell function in the cochlea. Oncomodulin (OCM) is a Ca2+ binding protein (CaBP) preferentially expressed in outer hair cells (OHCs) of the cochlea and few other specialized cell types. Here, we expand on our previous reports and show that OCM delays hearing loss in mice of two different genetic backgrounds: CBA/CaJ and C57Bl/6J. In both backgrounds, genetic disruption of Ocm leads to early progressive hearing loss as measured by auditory brainstem response (ABR) and distortion product otoacoustic emission (DPOAE). In both strains, loss of Ocm reduced hearing across lifetime (hearing span) by more than 50% relative to wild type (WT). Even though the two WT strains have very different hearing spans, OCM plays a considerable and similar role within their genetic environment to regulate hearing function. The accelerated age-related hearing loss (ARHL) of the Ocm KO illustrates the importance of Ca2+ signaling in maintaining hearing health. Manipulation of OCM and Ca2+ signaling may reveal important clues to the systems of function/dysfunction that lead to ARHL.
Insights
Oncomodulin (OCM), a calcium-binding protein, significantly delays age-related hearing loss in mice. Genetic absence of OCM accelerates hearing impairment, highlighting its critical role in maintaining cochlear function and auditory health.
Area of Science:
- Neuroscience
- Otolaryngology
- Genetics
Background:
- Calcium (Ca2+) signaling is crucial for cochlear sensory hair cell function.
- Oncomodulin (OCM), a calcium-binding protein, is highly expressed in cochlear outer hair cells (OHCs).
Purpose of the Study:
- To investigate the role of Oncomodulin (OCM) in age-related hearing loss (ARHL) across different mouse genetic backgrounds.
- To determine the impact of OCM deficiency on hearing function throughout the lifespan.
Main Methods:
- Auditory brainstem response (ABR) measurements to assess hearing thresholds.
- Distortion product otoacoustic emission (DPOAE) tests to evaluate outer hair cell function.
- Genetic analysis of OCM knockout (KO) mice compared to wild-type (WT) littermates in CBA/CaJ and C57Bl/6J strains.
Main Results:
- Genetic disruption of OCM (Ocm KO) led to early-onset, progressive hearing loss in both CBA/CaJ and C57Bl/6J mice.
- Loss of OCM reduced the hearing span by over 50% in Ocm KO mice compared to WT.
- OCM plays a significant and consistent role in regulating hearing function, irrespective of the genetic background's baseline hearing span.
Conclusions:
- OCM is essential for maintaining hearing health and delaying age-related hearing loss (ARHL).
- The accelerated ARHL in Ocm KO mice underscores the importance of Ca2+ signaling in the cochlea.
- Targeting OCM and Ca2+ signaling pathways may offer therapeutic strategies for ARHL.
